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Acta Physiologica 2012; Volume 206, Supplement 693
Joint FEPS and Spanish Physiological Society Scientific Congress 2012
9/8/2012-9/11/2012
Santiago de Compostela, Spain
ESTRADIOL INDUCES DIFFERENTIAL PRODUCTION OF CELL MEDIATORS IN ARTERIAL AND VENOUS ENDOTHELIAL CELLS
Abstract number: O418
Hermenegildo1 C, Bueno-Beti2 C, de Lazaro-Franco2 M, Martinez-Gil1 N, Perez-Cremades1 D, Monsalve1 E, Novella2 S
1Dep. Physiology, University of Valencia,
2Research Foundation - INCLIVA, Hospital Clnico de Valencia
Objectives:
Vascular effects of estradiol (E2) are induced by the release of endothelial mediators from nitric oxide (NO) and prostaglandin pathways. To explore these physiological pathways, the use of endothelial cells is widespread, despite the controversy about the impact of vascular bed origin on their function. Our aim was to compare the effects of E2 on NO, prostacyclin (PGI2) and thromboxane A2 (TXA2) production by human umbilical endothelial cells derived from vein (HUVEC) and artery (HUAEC).
Materials:
Cell cultures were exposed to physiological concentrations of E2 for 24h. NO was measured by amperometry. PGI2 and TXA2 were measured by ELISA. Role of estrogen receptors (ER) was studied with unspecific antagonist ICI182780 and specific ER alpha receptor antagonist (MPP). Endothelial NO synthase (eNOS), prostacyclin synthase (PGIS), cyclooxigenase-1 (COX-1) and -2 (COX-2) gene and protein expression were assessed by QRT-PCR and Western blot. One-way ANOVA followed by Bonferroni's post-test were used for statistical analysis.
Results:
In HUVEC, E2 increased NO (up to 153 %, p < 0.01) and PGI2 (up to 162 %, p < 0.05) production in a dose-dependent manner (0.01-10 nM) without any change in HUAEC. TXA2 production was unaltered in arterial or venous cells. Supporting these results, E2 increased the protein and gene expression of the enzymes involved in these pathways eNOS, COX-1 and PGIS only in HUVEC, whereas COX-2 did not change. Estradiol effects were completely abolished in the presence of ICI182780 and MPP.
Conclusions:
Release of protective vascular endothelial factors NO and PGI2 induced by E2 is typical in HUVEC through the activation of ER alpha, but not in HUAEC. This divergence is due to a deficit in gene and protein expression in response to estradiol in HUAEC and confirms the existence of behavioral differences of endothelial cells according to their origin.
Supported by Min. Economía y Competitividad (PRI-AIBDE-2011-0855), ISCIII (FIS 10/00518, RD06/0009), Cons. Educación, Gen. Valenciana (ACOMP/2012/218), Spain.
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 693 :O418